Ask about this productRelated genes to: PRKCE antibody
- Gene:
- PRKCE NIH gene
- Name:
- protein kinase C epsilon
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2016-01-27
Related products to: PRKCE antibody
Related articles to: PRKCE antibody
- Gualou Xiebai Banxia decoction (GXB) is a classic formula originated from "Synopsis of the Golden Chamber", with efficacy in activating cardiac "yang", resolving phlegm, and promoting blood circulation. Nearly 2000 years of clinical practice have demonstrated the efficacy of GXB in managing myocardial ischemia (MI). Nevertheless, its regulatory effects on metabolic disturbances associated with MI and the underlying mechanisms remain obscure. - Source: PubMed
Publication date: 2026/05/17
Zuo Li-HuaYang Sheng-JieZhang Zhi-BoHe Chen-HanWei Yu-JieAn Ya-RanZhao Song-FengSun ZhiLiu Li-Wei - Human neural organoids (NOs) provide a powerful platform for investigating synaptic development and dysfunction during early neurodevelopment. However, methodologies for isolating functional synaptic structures from these models remain limited. Here, we present a differential centrifugation protocol enabling the enrichment of growth cone particles (GCPs) and immature synaptosomes from air-liquid interface cerebral organoids (ALI-COs) at distinct developmental stages (Day 90 and 150). Notably, the method avoids density gradients, requires minimal starting material while maintaining reproducibility across human and murine tissues. Quantitative proteomic profiling revealed significant enrichment of growth cone markers (e.g., GAP43) and classical synaptosomal proteins (e.g., PCLO, BSN, SYN1). Transmission electron microscopy (TEM) confirmed the presence of membrane-enclosed GCPs with fibrous content and mitochondria in Day 90 isolates, and immature synaptosomes containing synaptic vesicles on day 150. Functional viability of both types of synaptic structures was demonstrated through KCl-induced depolarization, which triggered phosphorylation changes in growth cone proteins (GAP43, MARCKS, MARCKSL1), cytoskeletal regulators (DCLK1, SHTN1, MARK4, MAP1B) and protein kinases (CAMK2G, PRKCE) in Day 90 GCPs, as well as classical synaptic vesicle cycle proteins (SYN1, DNM1, RPH3A) at Day 150. Overall, this study establishes a centrifugation-based protocol for isolating growth cones and immature synapses from human organoids, capturing key stages of synaptic development and enabling scalable, patient-compatible models to study synaptic function and dysfunction in neurodevelopmental and neurodegenerative disorders. - Source: PubMed
Øhlenschlæger Marie SCriscuolo LucreziaJensen PiaLloyd-Davies Sánchez Daniel JSutcliffe MagdalenaBhosale SantoshBogetofte HelleTahir MuhammadJakobsen Lene APihl MariaBrewer JonathanSchwämmle VeitPoulsen Frantz RFreude KristineLancaster Madeline ARobinson Phillip JLarsen Martin R - The mechanism by which cigarette smoking affects bladder cancer susceptibility via glucose metabolism remains unclear. We identified bladder cancer-specific glucose metabolism-related genes (GMGs) using Molecular Signatures Database (MSigDB) and a case-control study (580 cases and 1,101 controls) through genetic association and interaction analyses with cigarette smoking. Among 811 GMGs, we observed that rs4953292 G > A was significantly associated with increased bladder cancer risk [odds ratio (OR) = 1.19, 95% confidence interval (CI): 1.03-1.37, = 1.87 × 10] and exhibited an interaction effect with cigarette smoking ( < 0.05). Smokers with rs4953292 A allele had higher bladder cancer risk than nonsmokers with G allele ( < 9.09 × 10). We performed functional experiments using 4-aminobiphenyl (4-ABP)-treated bladder cancer cells and found that the rs4953292 A allele combined with 4-ABP decreased expression levels in bladder cancer cells, which could upregulate PKG and phosphorylate VASP within the cGMP-PKG signaling pathway, enhance glucose uptake, lactate generation, and extracellular acidification rate (ECAR) to reprogram glycolysis, thus promoting bladder cancer susceptibility. This study elucidates that cigarette smoking-regulated facilitates bladder cancer susceptibility by mediating glycolytic reprogramming through activating the cGMP-PKG signaling pathway. The findings provide valuable predictors for bladder cancer susceptibility, aiding in prevention strategies. - Source: PubMed
Publication date: 2025/12/29
Xiao YanpingZhang JinyueJia YuSong HuiMao ZhenguangGao FangZheng Rui - Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related death, and patients usually exhibit impaired immune function within the tumor environment. NSD2 is an H3K36 methyltransferase and has been considered a cancer-promoting factor. However, the role of NSD2 in the occurrence and development of HCC is still unclear. In this study, the effects of NSD2 on HCC were assessed by both mouse and cell models. RNA-seq, ChIP-seq, and orthotopic tumor models were employed to decipher the downstream mechanisms of NSD2 responsible for HCC development. NSD2 alterations were characterized in patients with HCC. Hepatocyte-specific NSD2 overexpression suppresses the proliferation of tumor cells in DEN-treated mice. Mechanistically, NSD2 inhibits OXPHOS by activating target genes (Camk2d and Prkce) transcription. Downregulation of OXPHOS, caused by overexpression of NSD2, inhibits the expression of PD-L1 and enhances immune recognition of tumors. What's more, inhibition of OXPHOS suppresses the formation of HCC. Finally, patients with low expression of NSD2 have a better response to PD-L1 inhibitor treatment. These findings showed that NSD2 inhibits the progression of HCC by inhibiting the expression of PD-L1 through OXPHOS. Our results identify NSD2 as a tumor suppressor in the development of HCC. - Source: PubMed
Publication date: 2026/02/27
Zhang WeiFeng WenxinMa ChunxiaoRao HanyuLiu ChangweiXu YueLiu NingyuanWang ZiyiAji RebiguliHan TingGao Wei-QiangXiao XiuyingLi Li - Chronic joint pain in rheumatoid arthritis (RA) represents a persistent therapeutic challenge, and although luteolin (LUT) exhibits established anti-inflammatory properties, its precise mechanism for alleviating RA-associated chronic pain remains undefined. Through systematic investigation in collagen-induced arthritis (CIA) mice, we demonstrated that LUT administration effectively attenuated chronic pain by modulating spinal cluster of differentiation 4 positive T (CD4 T) cell dynamics and suppressing microglial activation. Integrated multi-omics profiling (cleavage under targets and tagmentation (CUT&Tag), RNA sequencing (RNA-seq), and metabolomics) coupled with functional validation revealed nuclear factor of activated T cells 2 (NFATC2) as the central transcriptional regulator governing T helper 17 (Th17) cell differentiation and spinal infiltration through protein kinase C epsilon (PRKCE)-signal transducer and activator of transcription 3 (STAT3) signaling transduction. Significantly, our mechanistic studies uncovered a previously unrecognized epigenetic cascade: LUT-mediated suppression of lactate dehydrogenase A (LDHA) activity disrupts glycolysis-fueled histone 3 lysine 9 lactylation (H3K9la), thereby epigenetically silencing NFATC2 transcription. Translational studies using RA patient-derived CD4 T cells confirmed LUT's capacity to normalize pathological hyperactivity of the LDHA/H3K9la/NFATC2 axis, concomitantly regulating CD4 T dynamics. Biophysical validation through molecular docking, surface plasmon resonance (SPR), and molecular dynamics (MD) simulations established LUT's direct binding to LDHA with high affinity. Collectively, these findings delineate a novel therapeutic paradigm wherein LUT alleviates RA-associated chronic pain by orchestrating Th17 differentiation and migratory capacity through coordinated blockade of the LDHA-H3K9la-NFATC2 signaling network, highlighting its potential as a disease-modifying agent for chronic pain management in RA. - Source: PubMed
Publication date: 2025/06/20
Jiang YuepengZhao YangMa XiaoZhao XiaoxuanZheng MengjiaWen JunjunYuan CunruiDing XinyiWen Chengping